EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c.
Oncogenesis
Xu L, Lin J, Deng W, Luo W, Huang Y, Liu CQ, Zhang FP, Qin YF, Wong PP, Liu C.
Publication Overview
Key findings, Countstar context, and access to the original paper.
2020
Cell Counting & Viability
No items found.
Key Finding
Silencing miR-200c rescued the tumorigenicity of EZH2-depleted HCC cells, whereas knocking down BMI1 reduced the promoting effect of miR-200c depletion on HCC cell migration. The findings demonstrated that alteration of EZH2 gene copy number status induced BMI1-mediated hepatocarcinogenesis via epigenetically silencing miR-200c, providing novel therapeutic targets for HCC treatment.
Countstar Connection
Cell numbers were assessed in the study's cell samples with Countstar (model not specified) during the study's growth assessment.
